FAICAR
Based on 1 Customer Validation
FAICAR (5-Formamidoimidazole-4-carboxamide ribotide) is a purine nucleotide and the IMP cyclohydrolase substrate of Cryptococcus neoformans ATIC. It is a key intermediate in the de novo purine synthesis pathway. FAICAR can be used in studies related to Cryptococcus neoformans infection.
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- Pureza : 85.0%
- No. CAS: 13018-54-7
- Fòrmula: C10H15N4O9P
- Peso molecular:366.22
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Almacenamiento:
-20°C, stored under nitrogen
* In solvent : -80°C, 6 months; -20°C, 1 month (stored under nitrogen)
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Actividad biológica
Descripciòn
In Vitro
FAICAR (0.005-0.3 mM) was used as substrate at 37°C, and recombinantly expressed C. neoformans ATIC exhibits IMP cyclohydrolase activity with a Km_app of 30 μM, Vmax of 8.6 U/mg, and kcat of 7.7 s−1[1].
FAICAR (0.1-4 μM) acts as a substrate for human AICAR transformylase-IMP cyclohydrolase's IMP cyclohydrolase domain, with a Ks of 0.87 μM at pH 7.4, and supports an IMP cyclohydrolase specific activity of 29.5 nmol IMP formed/min/μg protein at a concentration of 4 μM[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Chemical Information
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No. CAS 13018-54-7
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Appearance Solid
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Peso molecular 366.22
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Fòrmula C10H15N4O9P
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Color Dark purple to black
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SMILES
O=C(C1=C(NC=O)N([C@@H]2O[C@H](COP(O)(O)=O)[C@@H](O)[C@H]2O)C=N1)N
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Synonyms
5-Formamidoimidazole-4-carboxamide ribotide
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Structure Classification
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Initial Source
Methanocaldococcus jannaschii
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Envío
Room temperature in continental US; may vary elsewhere.
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Almacenamiento
-20°C, stored under nitrogen
* In solvent : -80°C, 6 months; -20°C, 1 month (stored under nitrogen)
Protocolo
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Research Protocol for Infectious Diseases
Infectious-disease experiments test how pathogens interact with host barriers, innate immune receptors, inflammatory signaling, pathogen replication, and tissue injury; pattern-recognition receptors such as TLRs, RIG-I-like receptors, NOD-like receptors, and inflammasomes detect microbial molecules and activate NF-κB, interferon, and cytokine responses. The central hypothesis is that infection severity reflects the balance between pathogen burden and host response: protective inflammation restricts pathogen growth, whereas excessive or mislocalized inflammation contributes to tissue damage and disease phenotype. Unresolved questions include which host pathways are protective versus pathogenic, why some infection models fail to translate to human disease, and which combined readouts best predict clinically relevant infection outcomes.
Pureza y Documentación
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Ficha de datos (307 KB)
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SDS (252 KB)
- English - EN (252 KB)
- Français - FR (252 KB)
- Deutsch - DE (252 KB)
- Norwegian - NO (252 KB)
- Español - ES (252 KB)
- Swedish - SV (252 KB)
- Italian - IT (252 KB)
- Korean - KR (252 KB)
- Portuguese - PT (252 KB)
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Instrucciones de manejo (2659 KB)
Referencias
[1]. Wizrah MSI, et al. AICAR transformylase/IMP cyclohydrolase (ATIC) is essential for de novo purine biosynthesis and infection by Cryptococcus neoformans. J Biol Chem. 2022;298(10):102453. [Content Brief]
[2]. Szabados E, et al. Radioassay of bifunctional 5-aminoimidazole-4-carboxamide ribotide transformylase-IMP cyclohydrolase by thin-layer chromatography. Anal Biochem. 1994;221(2):401-404. [Content Brief]
[3]. Vergis JM, et al. Catalytic mechanism of the cyclohydrolase activity of human aminoimidazole carboxamide ribonucleotide formyltransferase/inosine monophosphate cyclohydrolase. Biochemistry. 2004;43(5):1184-1192. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)